Hyperaminoacidemia from Interrupted Glucagon Signaling Increases Pancreatic Acinar Cell Proliferation and Size via mTORC1 and YAP/TAZ Pathways

By genetic and pharmacological disruption of glucagon receptor in mice and zebrafish, scientists reported that the ensuing hyperaminoacidemia promoted pancreatic acinar cell proliferation and cell hypertrophy, which could be mitigated by a low protein diet in mice.